By way of definition, in the field of automatic implantable arrhythmia control devices, the term "cardioversion" or "cardioverter" refers to the process of and device for discharging relatively high energy electrical shocks in excess of 1.0 Joule into or across cardiac tissue to arrest or "cardiovert" a tachyarrhythmia of a cardiac chamber. Delivery of cardioversion shocks may or may not be synchronized with a cardiac depolarization or rhythm and may be applied to arrest a malignant atrial or ventricular tachycardia or fibrillation with a selectable or programmable pulse energy. The termination of high rate tachycardias with lesser energy electrical pulses or bursts has also been referred to as "cardioversion" The arrest of atrial or ventricular fibrillation by higher energy shocks is referred to as "defibrillation", and defibrillation have been characterized in the past as a form of cardioversion. Products have been described and sold as "implantable cardioverter/defibrillator" (ICD) systems for providing synchronized cardioversion shocks or and unsynchronized defibrillation shocks and as "pacemaker/cardioverter/defibrillator" (PCD) systems for providing additional staged therapies of anti-tachyarrhythmia pacing, synchronized cardioversion shocks and unsynchronized defibrillation shocks. In the following description and claims, it is to be assumed that the terms "cardioversion" and "defibrillation" and variants thereof are interchangeable, and that use of one term is inclusive of the other device or operation, unless specific distinctions are drawn between them in the context of the use. For convenience, the term "cardioversion" or "cardioversion/defibrillation" will be used unless a form of defibrillation therapy is specifically referred to.
Tachyarrhythmias are episodes of high rate cardiac depolarizations, typically occurring in one chamber of the heart but which may be propagated from one chamber to the other, and are distinguished from sinus tachycardias that physiologically accompany exercise to provide adequate cardiac output. Tachyarrhythmias that are sufficiently high in rate and chaotic compromise cardiac output from the affected chamber(s), leading to loss of consciousness and death, in the case of ventricular fibrillation, or weakness and dizziness, in the case of atrial fibrillation or flutter and non-sinus atrial and ventricular tachycardias. Atrial fibrillation and flutter are debilitating, due to the loss of atrial cardiac output contribution and interference with ventricular filling, but not immediately life threatening unless it leads to ventricular fibrillation. High rate atrial and ventricular tachycardias may exhibit a more organized rhythm but also may disable the patient and can lead to fibrillation if untreated.
Fibrillation has generally been treated by means of high energy cardioversion/defibrillation shocks, which, in the context of implantable anti-arrhythmia devices, are applied by means of large surface area cardioversion electrodes, including an electrode on or in the chamber to be defibrillated. The battery life of an ICD or PCD device depends on the amount of energy expended in delivering a therapy and the delivery frequency. The high energy level employed in order to defibrillate consumes considerable energy in the range of 1.0-30.0 Joules per delivered shock. The high energy level is employed in order to simultaneously depolarize the bulk of the heart chamber to be defibrillated, which will include tissues in all stages of the depolarization-repolarization cycle at the time the pulse is delivered.
For patients experiencing ventricular fibrillation, the delivered cardioversion/defibrillation shock energy is necessary to save the patient's life and is usually not perceived by the patient because of the loss of consciousness shortly following onset of the arrhythmia. Accuracy of diagnosis and delivery of a cardioversion shock having sufficient energy to cardiovert the rhythm as quickly as possible are paramount concerns because the efficacy of the shock decreases with time lapse from onset of the symptoms.
Patients experiencing high rate atrial tachycardias and atrial fibrillation/flutter typically do not lose consciousness, and the condition is usually not life threatening. The intentional or inadvertent delivery of the cardioversion shock therapy by an ICD or PCD device is startling and painful to a degree that is assumed to be proportional to the shock energy level.
It was recognized early in the development of external ventricular defibrillators that a lower energy synchronous cardioversion shock could be employed to interrupt a high rate ventricular tachycardia, if the shock delivery was synchronized to a ventricular depolarization event, i.e. the R-wave. The lower energy threshold is attributed to the assumption that more of the ventricular muscle mass is intrinsically depolarized at this time, thereby requiring less cardioversion energy to depolarize the remaining ventricular muscle mass. If synchronization to a ventricular depolarization or R-wave peak can be achieved, staged therapy ICD and PCD devices deliver somewhat lower energy cardioversion shocks to the affected chamber. In such ventricular synchronous cardioversion, a delay interval of about 100 ms from the preceding R-wave peak is employed to ensure that the "vulnerable period" associated with the re-polarization of the heart is past.
Episodes of atrial tachyarrhythmias occur frequently and are debilitating to the patient, if not life threatening. Unfortunately, the quantity of electrical energy required to cardiovert or defibrillate the atria is sufficient, in most cases, to cause a sudden, propagated pain in the patient's chest area or to stun the patient. Typically reported defibrillation thresholds (in humans) of 2-3 Joules are required between transvenous lead bearing electrodes placed to provide atrial cardioversion pathways between the right atrium (RA) and the coronary sinus (CS) or the superior vena cava (SVC) and the CS. Other atrial electrode systems may require up to 4.-10 Joules (in humans) to reliably cardiovert. Significant discomfort and often intolerable pain is associated with such atrial cardioversion/defibrillation shock therapies in this range, resulting in sedation of some patients and refusal to accept the therapy by other patients. Moreover, there is concern that the attempt to defibrillate the atria will itself induce ventricular fibrillation leading to the death of the patient. In the hospital setting, the patient is carefully monitored, and induced ventricular fibrillation may be defibrillated. However, the clinical procedure still entails enough risk that drug therapies are preferred, and atrial defibrillation is used only after other therapies fail.
The same concerns have delayed the development of implantable atrial defibrillators so that patients prone to bouts of atrial fibrillation or flutter could remain ambulatory. One possible approach that has been widely published is to combine the atrial and ventricular fibrillation detection and cardioversion/defibrillation capabilities in a single implantable system so that induced ventricular fibrillation could be terminated. Such a device is disclosed in U.S. Pat. No. 5,549,642, issued to Min et al. The Incontrol Metrix TM atrial defibrillator, currently in clinical evaluation, does not provide the capability of treating induced ventricular tachyarrhythmias and therefore relies upon shock delivery criteria to avoid induction of ventricular tachyarrhythmias.
In the context of atrial cardioversion, a proposed pacemaker/defibrillator is disclosed in PCT Publication No. WO 92/18198 by Adams et al. where the synchronization of the high voltage atrial cardioversion shock is to the R-wave in an effort to avoid inducing ventricular tachycardia or fibrillation. In any case, synchronization to an R-wave in a high rate, irregular EGM has proven to be difficult to accomplish and not always effective to avoid inducing ventricular fibrillation.
Faced with these difficulties, attempts have been made to first make the cardiac rhythm more regular so that the P-wave or R-wave may be detected and to then apply the synchronous cardioversion therapy. In commonly assigned U.S. Pat. No. 5,193,536, a PCD system is described where the high atrial or ventricular rate is made more regular by delivering overdrive pacing pulses to capture the heart and by using the last overdrive pulse delivered as a synchronization event to time the delivery of the cardioversion shock. Another method is disclosed in U.S. Pat. No. 5,074,301 where a single pacing pulse is delivered to the atrium to allow the cardioversion shock to be delivered in the atrial refractory period. It is not suggested that the overdrive pacing pulses affect the cardioversion threshold.
In U.S. Pat. Nos. 5,314,448 and 5,366,485, an ICD is described having a set of cardioversion electrodes arranged around the patient's heart. When fibrillation is detected, the high output capacitors begin to be charged. As they are charged or after full charge is achieved, a "pre-treatment" of the fibrillating heart muscle is commenced through the generation of a train of pulses from the voltage on the output capacitors and delivery of the pulses across the cardioversion electrodes. The capacitors are recharged and at the end of the recharge time period, the high energy cardioversion pulse is delivered across the cardioversion electrodes. It is stated that the pre-treatment pulses begin the process of organizing the chaotically contracting myocardial cells and result in a reduction of cardioversion threshold and the total energy expended. It is emphasized that the pre-treatment pulse voltages are well in excess of pacing level voltages and that the same cardioversion electrodes are employed to deliver the energy to the same myocardial cells as will be defibrillated by the cardioversion pulse. In this manner, the pre-treatment pulses are delivered into the high current density regions of the current pathways in the heart chamber between the spaced apart cardioversion electrodes.
In the above-referenced '251 application, a method and apparatus for terminating fibrillation is disclosed using a burst of pacing energy, high frequency pulses applied into a low current density region of the cardiac tissue in the chamber in fibrillation prior to the delivery of one or more cardioversion energy pulses. The burst of pacing energy pulses is delivered between the pace/sense electrodes located in the low current density region of the cardioversion pathway around and through the heart chamber defined by the cardioversion energy distributed between the spaced apart cardioversion electrodes. The burst of pacing energy pulses injected into the low current density region results in the lowering of the cardioversion threshold, and the decreased energy cardioversion pulse effectively terminates the fibrillation episode. The burst of pacing energy pulses appears to develop a refractory island in the low energy region of the heart chamber that may itself lower the cardioversion energy, and also appears to prevent ectopic beats originating in the low energy region from re-fibrillating the heart.
Recently, the theoretical possibility of employing low energy pacing level pulses (i.e. less than 0.05 joules) to terminate atrial fibrillation has been explored. For example, in the recent article "Regional Control of Atrial Fibrillation by Rapid Pacing in Conscious Dogs", by Allessie et al, published in Circulation, Volume 84, No. 4, October 1991, pages 1689-1697, the ability of pacing pulses to capture a small area of fibrillating atrial tissue, if applied during a specified time interval synchronized to the sensed depolarization waveform at the pacing electrode site, is reported. However, the depolarization wavefront created by such pulses does not propagate through the entire chamber due to the varying polarization states of the tissue surrounding the stimulation site. Consequently, it has not been demonstrated that this approach can defibrillate a heart chamber actually in fibrillation.
It is generally believed that the delivery of pacing pulse bursts to the atrium can induce atrial fibrillation, unless the delivery is synchronized to P-waves to assure that the pulse bursts occur within the refractory period of the atrium. This effect is discussed in U.S. Pat. No. 5,334,221 which discloses a device which provides pulse bursts, synchronized to a P-wave, to the SA nodal fat pad in the atrium to reduce the sinus rate of patients who suffer from angina.
Despite this general belief, it has also been proposed to avoid synchronizing the delivered pacing pulse or burst to a detected depolarization to interrupt atrial fibrillation or flutter. In the '577 application, the pacing pulses are simultaneously delivered at multiple sites distributed over a substantial portion of the atria or atrium to be treated. Rather than attempt to synchronize the delivered pulses to the high rate atrial electrogram sensed at a stimulation site, simultaneous pulse delivery at the multiple dispersed sites is intended to eventually result in capture of the atrial tissue at one or more of the stimulation sites. It is theorized that the propagation of the depolarization wavefront created in response to the delivered pacing pulse, toward cardiac tissue closely adjacent the site at which capture initially occurs, increases the probability that the adjacent tissue will be in an appropriate stage of the depolarization-repolarization cycle to be captured by the next pulse in the burst. As pulses of the burst continue to be delivered, therefore, the amount of atrial tissue captured should gradually increase, with the end result of capturing a sufficient amount of atrial tissue to terminate fibrillation.
Similarly, in the '578 application, a series of low energy pulse bursts is delivered, separated by defined inter-burst intervals, and including bursts unsynchronized to atrial heart depolarizations. Detection of termination of atrial fibrillation during inter-burst intervals results in cancellation of further pulse bursts to prevent re-induction of fibrillation.
Despite these advances, a need continues to exist for atrial and ventricular cardioversion systems that can cardiovert high rate atrial and ventricular tachycardias and atrial fibrillation/flutter at lower energy levels to decrease energy consumption and pain perceived by the patient.